Morphological changes in subcutaneous and peri-articular tissues in the foot and lower leg are best assessed using in-vivo imaging techniques. With high resolution ultrasonography the geometric boundaries of superficial structures in the foot and lower leg can be assessed, from which tissue thickness can be measured (D’Ambrogi et al. 2003; Giacomozzi et al. 2005). More detailed qualitative and quantitative information of superficial and deep structures can be obtained using magnetic resonance imaging (MRI). MRI is superior to other imaging techniques in distinguishing soft tissue such as muscle, tendon, ligament, fascia, and fat, and can be used to measure tissue thickness and assess the presence of rupture. The plantar fascia can be tested functionally using Jack’s test, in which the hallux is passively dorsiflexed while weight-bearing (Chuter & Payne 2001). A normal response is tightening of the fascia and a raise of the foot arch. Failure may indicate fascia dysfunction or rupture.

The so called “prayer sign” was originally used to classify patients with limited joint mobility (LJM). This is present when the patient fails to approximate the metacarpal–phalangeal joints while opposing the palmar surfaces of the hands in a praying position. Although this method is simple in use, it is not a direct measure of LJM in the foot. Typically, a goniometer is used to assess mobility of the foot and ankle joints in a nonweightbearing position. Goniometric measurements of joint mobility are quite reliable, with reported coefficients of variation of 8.5% for the subtalar joint and 7.4% to 11.0% for the first metatarsal–phalangeal (MTP) joint (Delbridge et al. 1988; Zimny et al. 2004). Mobility and stiffness of the first MTP joint can be assessed using a mechanical testing device (Birke et al. 1995). Joint stiffness can be calculated from vertical displacement of the first metatarsal head plotted against the applied force to the metatarsal head.

Biomechanical function of the foot is most often assessed in diabetic patients by measuring the dynamic pressure distribution underneath the foot. Patients walk barefoot across a platform, which consists of a matrix of hundreds to thousands of sensors measuring vertical pressure. Most often the peak pressure and the time integral of this peak pressure are calculated for multiple anatomical regions in the foot, so that conclusions on local pressure effects can be drawn.

The plantar fascia of diabetic patients with claw toe deformity showed discontinuity, indicating rupture, in one MRI study (Taylor et al. 1998). The authors suggest that the effects of nonenzymatic glycosylation may render the aponeurosis less compliant and more prone to rupture. However, none of the patients with claw toe deformity in another MRI study showed discontinuity of the aponeurosis (Fig. 5.5.1) (Bus 2004). Also, signal intensity increases and substantial thickening of the aponeurosis at the calcaneal insertion compatible with plantar fasciitis have been found in neuropathic diabetic patients. However, these changes did not differentiate patients with toe deformity from those without (Bus 2004). Clearly, the data on fascia rupture and the role the aponeurosis plays in causing toe deformity in diabetic patients remain inconclusive.

The plantar fascia may be thicker in diabetic patients than in healthy controls (D’Ambrogi et al. 2003; Bolton et al. 2005). High-resolution ultrasound images showed on average 2.0 mm thickness at the calcaneal insertion in healthy controls, 2.9 mm in diabetic patients, 3.0 mm in neuropathic diabetic patients, and 3.1 mm in diabetic patients with a history of foot ulceration (D’Ambrogi et al. 2003). With computed tomography, a thicker aponeurosis was found in diabetic patients than in healthy controls (mean 4.2 vs 3.6 mm) (Bolton et al. 2005). Increased fascia thickness in diabetes is likely also associated with nonenzymatic glycosylation of collagen; a reduction of 30% in collagen content in the plantar fascia has been found in diabetic patients (Andreassen et al. 1981). Apparently, with long-standing diabetes, geometric changes of the plantar fascia shown as thickening of this connective tissue structure may occur.

Thickening of plantar fascia can influence biomechanical foot function in diabetes. Dynamic forefoot pressures were found to be significantly higher in diabetic patients with thicker plantar fascia than in diabetic and healthy control subjects with thinner plantar fascia (D’Ambrogi et al. 2003; Giacomozzi et al. 2005). Additionally, a significant correlation (r  =  0.52) was found between fascia thickness and forefoot pressure in these patients. This association may be explained by the role plantar fascia plays in countering the flattening of the foot during mid-stance of gait. The vertical forces acting on the forefoot during arch flattening are countered by horizontal forces generated in passive structures such as the plantar fascia, which try to tie the forefoot and rearfoot together. With fascia thickening, resistance increases, meaning that larger vertical forces measured as higher pressures are required at the forefoot in order to flatten the foot during stance.

In patients with Charcot’s neuroarthropathy, plantar fascia dysfunction or rupture may be indicated, based on a negative response to Jack’s test (Chuter & Payne 2001). Additionally, rupture of the plantar fascia has been suggested as a potential factor in the increased forefoot-to-rearfoot pressure ratio that is found in neuropathic diabetic patients when compared to healthy controls (Caselli et al. 2002). A suggested forefoot drop as a result of fascia rupture (Sharkey et al. 1999), may cause increased loading in the forefoot and explain these results. More research is required to improve our understanding of the role that the plantar fascia plays in altering biomechanical function of the foot in diabetes.

The clinical implications of structural changes in the plantar fascia in diabetic patients are not known. This may be the reason for the paucity of data on treatment options. Alterations in foot function associated with plantar fascia dysfunction may be indicative of its contributing role in foot ulceration in diabetic patients (Caselli et al. 2002; D’Ambrogi et al. 2003). However, direct assessments of this relationship have not been made to date.